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M Gellai

Publications and source records attributed to M Gellai.

66 records · Page 4Linked to original sources
PubMed1982

The role of vasopressin in the control of renal hemodynamics. The Brattleboro rat as an experimental model.

It has been demonstrated through the use of new techniques that the action of vasopressin on the kidneys is not limited to changing the water permeability of distal tubules and collecting ducts. However, it has yet to be established whether these additional actions, such as lowering Kf (possibly by contracting mesangial cells), or increasing postglomerular vascular resistance, are important factors in the control of GFR and renal blood flow. The use of animals with diabetes insipidus, particularly the Brattleboro homozygous (DI) rat, may help to circumvent a number of methodological problems and provide a useful model for assessing the role of vasopressin in the control of renal hemodynamics. Although that role may be exerted through a direct effect on the vascular tone, it may be an indirect effect in which the antidiuretic action of vasopressin alters fluid balance and elicits secondary changes in other vasoactive hormones. The complexity of this latter possibility suggests that other methodological problems (in the measurement and/or control of the related variables) may complicate the final resolution of this issue for some time to come.

Animals↗
PubMed1982

Replacement therapy with arginine vasopressin in homozygous Brattleboro rats.

We studied the replacement therapy of different doses of AVP in DI rats. It is surprising that relatively high levels of plasma AVP were needed to achieve significant antidiuretic effects. Measured plasma AVP concentrations are less than those predicted from the release rates of AVP by the minipumps. This difference may be due to the subcutaneous mode of release of AVP. The study also provides evidence that urinary excretion of AVP is a good indicator of the plasma AVP level.

Animals↗
PubMed1981

Demonstration that rat prolactin has no intrinsic antidiuretic activity in the rat.

The proposition that rat prolactin has an intrinsic antidiuretic activity was examined using a conscious rat model (Brattleboro homozygotes, DI rats) which does not appear to produce arginine vasopressin (AVP). A preparation of rat prolactin obtained from NIAMDD, rat prolactin B1, produced a prompt antidiuresis when administered intravenously to these animals. Prolactin B1 was found to contain 150 ng of AVP/mg protein by RIA. All of the measurable AVP was removed from prolactin B1 by polyacrylamide gel electrophoresis and the electrophoresed prolactin was completely devoid of any antidiuretic activity. Addition of synthetic AVP to electrophoresed prolactin in an amount equivalent to the AVP contamination of prolactin B1 completely restored the originally observed antidiuretic activity. Synthetic AVP given alone produced a similar antidiuresis, but in the presence of electrophoresed prolactin these effects were produced by much smaller amounts of AVP. We believe that our data demonstrate that rat prolactin has no intrinsic antidiuretic activity, and that the antidiuretic activity associated with different prolactin preparations could be entirely due to their contamination with AVP. The data also show that the presence of prolactin enhanced by about five times the antidiuretic activity of AVP.

Animals↗
PubMed1980

Concentration of urine in the absence of ADH with minimal or no decrease in GFR.

It is known that large (more than 50%) reductions in glomerular filtration rate (GFR) can lead to formation of hyperosmotic urine in the absence to depend critically upon reduced delivery of luid to the loops of Henle. In the present study, we tried to determine whether a much lesser decrease in GFR could also result in hyperosmotic urine when ADH is absent. The following mean values (control vs. 3 h of partial aortic constriction) were obtained in 21 conscious diabetes insipidus rats: GRF, 909 +/- 35 (SE) vs. 835 +/- 49 microliter . min-1 . 100 g body wt-1 (8% decrease; P less than 0.02); urinary osmolality (Uosmol), 125 +/- 6 vs. 309 +/- 14 mosmol/kg H2O (P less than 0.001; peak Uosmol 350 +/- 22). Analysis of individual responses revealed that Uosmol increased as much when there was no measurable decrease in GFR as when such decrease occurred. Neither GFR nor filtration fraction bore any systematic relationship to Uosmol or to each other. We conclude that in the absence of ADH Uosmol can increase with minimal or no change in GFR. Changes in filtration fraction--a potential mediator of reduced delivery to the loops--could not explain the increased Uosmol, even in those instances in which GFR remained unchanged.

Animals↗
PubMed1979

Urinary concentrating ability during dehydration in the absence of vasopressin.

Despite the apparent absence of vasopressin (ADH), Brattleboro homozygotes [diabetes insipidus (DI) rats] can concentrate their urine when deprived of drinking water. Since other investigators have shown that reducing glomerular filtration rate (GFR) improves the concentrating ability of water-loaded dogs, the present studies were undertaken to quantify the magnitude and time course of changes in GFR during dehydration. Clearance experiments were performed in 10 conscious DI rats before and following 3, 6, 9, 12, 15, and 24 h of dehydration. Urine osmolality increased from 155.0 +/- 12.6 (SE) to 696.7 +/- 8.4 mosmol/kg H2O after 24 h. GFR averaged 984.3 +/- 79.6 microliters . min-1 . 100 g body wt-1 in the control phase, fell to about 80% of this value over the first 12 h of dehydration, and then declined to 27% at 24 h. The rats lost 20% of their body weight over the 24 h. The osmolality of the papillary tip averaged 896 +/- 44 mosmol/kg H2O at 24 h compared to a control value of 493 +/- 28. The lack of osmotic equilibration between urine and papillary interstitium suggests that dehydration did not appreciably increase the water permeability of the distal nephron. These experiments clearly show a progressive decline in GFR as urine becomes concentrated during dehydration in the absence of ADH; these events may or may not be causally related.

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